This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. All pathogens struggle to obtain iron from the host bloodstream, whereas commensal organisms of the mammalian gastrointestinal tract must struggle with a surfeit of iron. The commensal-pathogenic yeast Candida albicans manages to succeed in both environments through previously unknown mechanisms. We discovered that unlike other model organisms like S. pombe, C. albicans inserts a transcriptional activator called Sef1 between two more broadly conserved transcriptional regulators, a repressor of iron uptake genes called Sfu1 and a repressor of iron utilization genes called Hap43. These three transcription factors form a feed-forward circuit that is distinct from those described in nonpathogenic model yeasts. Interesting, we found that Sef1 undergoes post-transcriptional modification when the cells are shift from high iron to low iron environments and our preliminary results suggest that phosphorylation may contribute to this modification. Mapping Sef1 phosphorylation will yield insight into the mechanisms regulating iron acquisition in this commensal-pathogenic yeast.